2004 Progress Report: St. Louis Bus, Steubenville and Atlanta Studies

EPA Grant Number: R827353C003
Subproject: this is subproject number 003 , established and managed by the Center Director under grant R827353
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: EPA Harvard Center for Ambient Particle Health Effects
Center Director: Koutrakis, Petros
Title: St. Louis Bus, Steubenville and Atlanta Studies
Investigators: Gold, Diane R. , Koutrakis, Petros , Stone, Peter , Suh, Helen H.
Current Investigators: Gold, Diane R. , Adamkiewicz, Gary , Coull, Brent , Dockery, Douglas W. , Dubowsky, S. , Luttmann-Gibson, Heike , Sarnat, Jeremy , Schwartz, Joel , Stone, Peter , Suh, Helen H. , Wheeler, A. , Zanobetti, Antonella
Institution: Harvard University
Current Institution: Harvard T.H. Chan School of Public Health , Harvard University
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
Project Period Covered by this Report: June 1, 2004 through May 31, 2005
Project Amount: Refer to main center abstract for funding details.
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text |  Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air


In the 6th Year of our Center, we analyze data collected in our St. Louis Bus Study to examine the effects of ambient and traffic related pollution on intermediate cardiovascular and inflammatory health markers, including heart rate variability, systemic inflammation, and pulmonary inflammation. Results from the analyses are presented below.

Progress Summary:

Heart Rate Variability

Exposure to airborne particles may increase cardiac risk by altering autonomic balance. As these risks may be particularly great for traffic-related particles, we examined associations between particles and heart rate variability for 44 subjects who participated in 4 repeated trips aboard a diesel bus. Twenty-four hour electrocardiograms were correlated with continuous particle concentrations using generalized additive models controlled for subject, weekday, time, apparent temperature, trip type, activity, medications, and autoregressive terms. Associations were assessed for short and medium-term mean concentrations.

Heart rate variability was significantly and negatively associated with fine particulate matter. Significant positive associations were demonstrated with heart rate and the low to high frequency power ratio. Associations were strongest with 24-hour mean concentrations although strong and significant short-term associations also were found during bus periods, independent of daily exposures. Overall, associations were largest for high frequency power with 16 (95% CI: -17, –15), 19 (95% CI: -22, –17), and 14 (95% CI: -16, –13) percent decreases per inter-quartile changes in the 24-hour PM2.5 (4.6 µg/m3), black carbon (458 ng/m3), and fine particle count (39 pt/cm3) concentrations, respectively. Eleven percent (95% CI: -13.6, –7.8) decreases in high frequency power were predicted per inter-quartile change in the 5-minute PM2.5 (10 µg/m3) aboard the bus. This investigation indicates that fine particles are negatively associated with heart rate variability, with an overall trend towards reduced parasympathetic tone. While daily associations were evident for all particles, short-term associations were predominantly limited to bus periods and possibly fresh traffic-related particles. A manuscript of these findings has been prepared and will be submitted to Environmental Health Perspectives in October 2005.

Systemic Inflammation

Inflammation may represent a pathway through which airborne particles lead to increased cardiac risk. Therefore, we investigated associations between ambient particles and acute systemic inflammation among repeated measures of 44 seniors and examined susceptibility by conditions linked to chronic inflammation. Mixed models were used to identify associations between fine particle concentrations (PM2.5) averaged over 1 to 7 days and measures of C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cell counts (WBC). Effect modification was investigated for diabetes, obesity, hypertension, and elevated mean inflammatory markers.

Positive associations were consistently found between ambient PM2.5 and WBC across all participants, with an 11% (95% CI: 0.19 to 22%) increase per 10 µg/m3 increase in PM2.5 averaged over the previous week. PM2.5 and CRP also exhibited positive associations among all individuals for averaging periods longer than 1 day with the strongest associations for persons with diabetes, obesity, and hypertension. For example, a 10 µg/m3 increase in the 5 day mean PM2.5 was associated with a 24 percent increase in CRP (95% CI: -8.8 to 67%) for all individuals and a 170 percent (95% CI: 36 to 420%) increase for persons with diabetes, obesity, and hypertension. Persons with diabetes, obesity, and hypertension also exhibited positive associations between PM2.5 and IL-6. Individuals with elevated mean inflammatory markers exhibited enhanced responsiveness for CRP, IL-6, and WBC. This investigation demonstrates that air pollution is positively associated with acute systemic inflammation and indicates enhanced sensitivity for individuals with diabetes, obesity, hypertension, and elevated mean inflammatory markers. A manuscript of these findings has been submitted to Environmental Health Perspectives.

Pulmonary Inflammation

Airborne particles have been linked to pulmonary oxidative stress and inflammation. As these effects may be particularly great for traffic-related particles, we examined associations between particle exposures and exhaled nitric oxide (FENO) in a study of 44 seniors, which involved repeated trips aboard a diesel bus. Samples of FENO collected before and after the trips were correlated with micro-environmental and ambient particle concentrations using mixed models controlled for subject, day, trip, vitamins, collection device, mold, pollen, room air nitric oxide, apparent temperature, and time to analysis. While ambient concentrations were collected at a fixed location, continuous group-level personal samples characterized micro-environmental exposures throughout facility and trip periods.

In pre-trip samples, both micro-environmental and ambient exposures to fine particles were positively associated with FENO. For example, an inter-quartile increase of 5.8 μg/m3 in the daily micro-environmental PM2.5 concentration was associated with a 10% (95% CI: 2 to 20) increase in FENO. After the trips, however, FENO concentrations were associated only with micro-environmental exposures, with significant associations for concentrations measured throughout the whole trip day and only during bus periods. Associations with bus exposures were strong and statistically significant with an 18 percent (95% CI: 11 to 26) increase in FENO predicted per inter-quartile increase of 8.4 μg/m3 in PM2.5. Although pre-trip findings were generally robust, our post-trip findings were sensitive to several influential days. Fine particle exposures may result in airway inflammation in senior adults, with associations best assessed by micro-environmental exposure measurements during periods of high particle exposures. A manuscript describing these findings is currently in the final stages of preparation.

Journal Articles:

No journal articles submitted with this report: View all 8 publications for this subproject

Supplemental Keywords:

exposure, health effects, susceptibility, metals, public policy, biology, engineering, epidemiology, toxicology, environmental chemistry, monitoring, air pollutants, air pollution, air quality, ambient air, ambient air monitoring, ambient air quality, ambient measurement methods, ambient monitoring, ambient particle health effects, ambient particles, animal inhalation study, assessment of exposure, biological mechanism, biological response, cardiopulmonary, cardiopulmonary response, cardiovascular disease, chemical exposure, children, developmental effects, dosimetry, environmental health hazard, exposure and effects, genetic susceptibility, health risks, human exposure, human health, human health effects, human health risk, human susceptibility, indoor air quality, indoor exposure, inhalation, inhalation toxicology, inhaled particles, lead, measurement methods, particle exposure, particulate exposure, particulates, pulmonary, pulmonary disease, respiratory, respiratory disease, risk assessment, sensitive populations, stratospheric ozone,, RFA, Health, Scientific Discipline, Air, particulate matter, Toxicology, air toxics, Environmental Chemistry, Epidemiology, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, indoor air, genetic susceptability, tropospheric ozone, Biology, ambient air quality, health effects, monitoring, risk assessment, sensitive populations, particulates, chemical exposure, interindividual variability, molecular epidemiology, air pollutants, exposure and effects, stratospheric ozone, ambient air monitoring, health risks, cardiopulmonary responses, indoor exposure, human health effects, ambient air, developmental effects, epidemelogy, respiratory disease, exposure, pulmonary disease, ambient measurement methods, ambient monitoring, air pollution, particle exposure, biological mechanism , Human Health Risk Assessment, human exposure, inhalation, pulmonary, ambient particle health effects, cardiopulmonary response, particulate exposure, inhaled, inhalation toxicology, human susceptibility, differentiating outdoor and indoor sources, atmospheric monitoring, cardiopulmonary, human health, indoor air quality, inhaled particles, measurement methods , metals, respiratory, genetic susceptibility, air quality, dosimetry, cardiovascular disease, human health risk

Progress and Final Reports:

Original Abstract
  • 1999 Progress Report
  • 2000 Progress Report
  • 2001 Progress Report
  • 2002 Progress Report
  • 2003 Progress Report
  • Final Report

  • Main Center Abstract and Reports:

    R827353    EPA Harvard Center for Ambient Particle Health Effects

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R827353C001 Assessing Human Exposures to Particulate and Gaseous Air Pollutants
    R827353C002 Quantifying Exposure Error and its Effect on Epidemiological Studies
    R827353C003 St. Louis Bus, Steubenville and Atlanta Studies
    R827353C004 Examining Conditions That Predispose Towards Acute Adverse Effects of Particulate Exposures
    R827353C005 Assessing Life-Shortening Associated with Exposure to Particulate Matter
    R827353C006 Investigating Chronic Effects of Exposure to Particulate Matter
    R827353C007 Determining the Effects of Particle Characteristics on Respiratory Health of Children
    R827353C008 Differentiating the Roles of Particle Size, Particle Composition, and Gaseous Co-Pollutants on Cardiac Ischemia
    R827353C009 Assessing Deposition of Ambient Particles in the Lung
    R827353C010 Relating Changes in Blood Viscosity, Other Clotting Parameters, Heart Rate, and Heart Rate Variability to Particulate and Criteria Gas Exposures
    R827353C011 Studies of Oxidant Mechanisms
    R827353C012 Modeling Relationships Between Mobile Source Particle Emissions and Population Exposures
    R827353C013 Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) Study
    R827353C014 Identifying the Physical and Chemical Properties of Particulate Matter Responsible for the Observed Adverse Health Effects
    R827353C015 Research Coordination Core
    R827353C016 Analytical and Facilities Core
    R827353C017 Technology Development and Transfer Core